作者: Etsuko Suzuki , Takashi Okada
DOI: 10.1111/J.1460-9568.2012.08127.X
关键词: Stimulation 、 Neuroscience 、 Long-term potentiation 、 Schaffer collateral 、 Synaptic plasticity 、 Acetylcholine 、 Neurotransmission 、 Biophysics 、 Tetanic stimulation 、 Muscarinic acetylcholine receptor 、 Chemistry
摘要: Acetylcholine is considered to be an endogenous modulator of hippocampal neurotransmission and synaptic plasticity. The activation muscarinic acetylcholine receptors (mAChRs) reportedly enhances plasticity, which plays important role in memory function; however, the mechanism by it plasticity remains unclear. Here, we examined involvement inhibition Kv7/M K(+) channels, are targets mAChR modulation, during activation-induced enhancement long-term potentiation (LTP) at rat Schaffer collateral (SC)-CA1 synapses. When electrical stimulus was applied stratum oriens before tetanic stimulation SCs, magnitude induced SC-CA1 synapse LTP enhanced as compared with that without stimulation. In presence antagonist atropine, stable LTP, but stimulation-evoked abolished. additional application XE991, a selective blocker rescued atropine-induced enhancement. phospholipase C (PLC) inhibitor U-73122 inhibited LTP. Application T/R-type voltage-dependent Ca(2+) channel (VDCC) Ni(2+) abolished addition, preceding able induce N-methyl-d-aspartate receptor blockade. We therefore propose inhibits channels through PLC activation, leads VDCC hence causes sufficient influx enhance